miRNA-99b-3p functions as a potential tumor suppressor by targeting glycogen synthase kinase-3β in oral squamous cell carcinoma Tca-8113 cells
Author(s) -
Kang He,
Dongdong Tong,
Si Zhang,
Donghui Cai,
Lumin Wang,
Yang Yang,
Ling Gao,
Sue Chang,
Bo Guo,
Tusheng Song,
Ang Li,
Chen Huang
Publication year - 2015
Publication title -
international journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2015.3135
Subject(s) - ectopic expression , cyclin dependent kinase 6 , biology , cancer research , gsk 3 , gene silencing , cyclin d1 , carcinogenesis , oncogene , microrna , cell cycle , cell growth , kinase , cell , downregulation and upregulation , gsk3b , cancer , cell culture , microbiology and biotechnology , gene , biochemistry , genetics
Dysregulation of microRNAs (miRNAs) has been associated with carcinogenesis in oral squamous cell carcinoma (OSCC). In the present study, we investigated the expression and function of miR-99b-3p in human OSCC. We found that the expression levels of miR-99b-3p decreased in 21 clinical OSCC samples (84%). Furthermore, ectopic expression of miR-99b-3p inhibited OSCC cell proliferation by downregulating glycogen synthase kinase-3β (GSK3β), an miR-99b-3p' target gene, at the mRNA and protein levels, both in vitro and in vivo. Moreover, the silencing of GSK3β recapitulated the cellular and molecular effects in a similar manner to the overexpression of miR-99b-3p, which included inhibition of OSCC cell proliferation and suppression of p65 (RelA) and G1 regulators (cyclin D1, CDK4 and CDK6) in vitro. Our data suggest that miR-99b-3p functions as a tumor suppressor in OSCC via GSK3β downregulation.
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